The role of the parasympathetic system in the control of insulin release in the conscious calf.

Abstract

SUMMARY1. The effect of atropine (0-2 mg/kg) on the release of insulin from the pancreas, in response to both exogenous and endogenous hyperglycaemia, has been investigated in conscious 2-to 5-week-old calves.2. The rise in mean plasma insulin concentration in response to infusions ofglucose, which raised the concentration of glucose in the plasma by about 4 0 mmol/l, was significantly depressed in calves with cut splanchnic nerves by prior administration of atropine.3. The rise in plasma insulin concentration, which normally follows stimulation of the splanchnic nerves in the conscious calf , was almost completely suppressed by prior administration of atropine.4. These findings are discussed in relation to those of other workers with other species. The results indicate that the parasympathetic innervation to the pancreas plays an important part in the control ofinsulin release in response to hyperglycaemia.

The role of the sympathetic system in the control of insulin release in response to hyperglycaemia in conscious calves.

“…infusions of exogenous glucose in conscious calves, which had been pre-treated with adrenergic blocking agents, with those which had previously been obtained in normal animals of the same age (Bloom & Edwards, 1981). No behavioural changes were observed which could be attributed to the administration of glucose or either pharmacological blocking agent.…”

“…min for the next 25 min. In addition the same dose of glucose was administered to two normal calves under precisely similar conditions to those employed previously (Bloom & Edwards, 1981) and the responses found to be closely similar. For financial and ethical reasons this earlier group was therefore taken as the control group for the purpose of comparisons.…”

“…The fact that i.v. infusions of exogenous glucose elicit the usual rise in mean plasma insulin concentration in calves with cut splanchnic nerves (Bloom & Edwards, 1981), and in animals pre-treated with both phentolamine and propranolol, whereas the response is suppressed by the administration of propranolol alone indicates that insulin release is prevented by unopposed cx-adrenergic inhibition (Porte, 1967 a). This is clearly an extremely potent effect as it completely suppresses release of insulin while the plasma glucose concentration is raised more than twofold, which is well beyond the normal physiological range.…”

“…The release of insulin which normally occurs during either exogenous or endogenous hyperglycaemia in the conscious calf is greatly reduced by pre-treatment with atropine whereas prior section of both splanchnic nerves does not appear to affect the response (Bloom & Edwards, 1981). This and other evidence (reviewed by Edwards, 1984) has led to the conclusion that pancreatic endocrine responses to ' glycaemic' stimuli are mediated, at least in part, by the parasympathetic innervation and that the role of the sympathetic system is restricted to effecting responses which occur during exercise or stress.…”

Pancreatic endocrine function in cortisol‐treated thyroidectomized calves.

“…R. BLOOM, A. V. EDWARDS AND A. S. FIELDING results in a severe diabetic syndrome after 2-3 weeks (Comline, Edwards & Nathanielsz, 1970;Edwards, Nathanielsz & Vaughan, 1971). Pancreatic endocrine responses to glycaemic stimuli are mediated largely via the parasympathetic innervation to the pancreas under normal conditions in this species (Bloom, Edwards & Vaughan, 1974;Bloom, Edwards & Hardy, 1978a, b;Bloom, Edwards & Jirhult, 1980;Bloom & Edwards, 1981;Edwards & Bloom, 1978) and this pathway can readily be activated by the administration of 2-deoxyglucose (Bloom et al 1978b(Bloom et al , 1980.…”